Suppression of the Schizosaccharomyces pombe cut12.1 cell-cycle defect by mutations in cdc25 and genes involved in transcriptional and translational control.

2.50
Hdl Handle:
http://hdl.handle.net/10541/71916
Title:
Suppression of the Schizosaccharomyces pombe cut12.1 cell-cycle defect by mutations in cdc25 and genes involved in transcriptional and translational control.
Authors:
Tallada, Victor A; Bridge, Alan J; Emery, Patrick A; Hagan, Iain M
Abstract:
Cdc25 phosphatase primes entry to mitosis by removing the inhibitory phosphate that is transferred to mitosis promoting factor (MPF) by Wee1 related kinases. A positive feedback loop then boosts Cdc25 and represses Wee1 activities to drive full-scale MPF activation and commitment to mitosis. Dominant mutations in the Schizosaccharomyces pombe spindle pole body (SPB) component Cut12 enable cdc25.22 mutants to overcome a G2 arrest at 36 degrees and enter mitosis. The recessive temperature-sensitive cut12.1 mutation results in the formation of monopolar spindles in which the spindle pole marker Sad1 is enriched on the nonfunctional SPB at 36 degrees . We identified mutations at five loci that suppressed the lethality of the recessive cut12.1 mutation at 36 degrees and conferred lethality at 20 degrees . Three of the five mutations led to the formation of monopolar spindles at restrictive temperatures, affected cell size at commitment to mitosis, and generated multiple Sad1 foci at nuclear periphery. The five loci, tfb2.rt1, tfb5.rt5, pla1.rt3, rpl4301.rt4, and rot2.1, and multicopy suppressors, including tfb1(+) and dbp10(+), are involved in transcription, translation, or RNA processing, prompting us to establish that elevating Cdc25 levels with the dominant cdc25.d1 allele, suppressed cut12.1. Thus, rot mutants provide a further link between protein production and cell-cycle progression.
Affiliation:
CRUK Cell Division Group, Paterson Institute for Cancer Research, University of Manchester, Manchester M20 4BX, United Kingdom.
Citation:
Suppression of the Schizosaccharomyces pombe cut12.1 cell-cycle defect by mutations in cdc25 and genes involved in transcriptional and translational control. 2007, 176 (1):73-83 Genetics
Journal:
Genetics
Issue Date:
May-2007
URI:
http://hdl.handle.net/10541/71916
DOI:
10.1534/genetics.107.072090
PubMed ID:
17409062
Type:
Article
Language:
en
ISSN:
0016-6731
Appears in Collections:
All Paterson Institute for Cancer Research

Full metadata record

DC FieldValue Language
dc.contributor.authorTallada, Victor A-
dc.contributor.authorBridge, Alan J-
dc.contributor.authorEmery, Patrick A-
dc.contributor.authorHagan, Iain M-
dc.date.accessioned2009-06-30T10:47:25Z-
dc.date.available2009-06-30T10:47:25Z-
dc.date.issued2007-05-
dc.identifier.citationSuppression of the Schizosaccharomyces pombe cut12.1 cell-cycle defect by mutations in cdc25 and genes involved in transcriptional and translational control. 2007, 176 (1):73-83 Geneticsen
dc.identifier.issn0016-6731-
dc.identifier.pmid17409062-
dc.identifier.doi10.1534/genetics.107.072090-
dc.identifier.urihttp://hdl.handle.net/10541/71916-
dc.description.abstractCdc25 phosphatase primes entry to mitosis by removing the inhibitory phosphate that is transferred to mitosis promoting factor (MPF) by Wee1 related kinases. A positive feedback loop then boosts Cdc25 and represses Wee1 activities to drive full-scale MPF activation and commitment to mitosis. Dominant mutations in the Schizosaccharomyces pombe spindle pole body (SPB) component Cut12 enable cdc25.22 mutants to overcome a G2 arrest at 36 degrees and enter mitosis. The recessive temperature-sensitive cut12.1 mutation results in the formation of monopolar spindles in which the spindle pole marker Sad1 is enriched on the nonfunctional SPB at 36 degrees . We identified mutations at five loci that suppressed the lethality of the recessive cut12.1 mutation at 36 degrees and conferred lethality at 20 degrees . Three of the five mutations led to the formation of monopolar spindles at restrictive temperatures, affected cell size at commitment to mitosis, and generated multiple Sad1 foci at nuclear periphery. The five loci, tfb2.rt1, tfb5.rt5, pla1.rt3, rpl4301.rt4, and rot2.1, and multicopy suppressors, including tfb1(+) and dbp10(+), are involved in transcription, translation, or RNA processing, prompting us to establish that elevating Cdc25 levels with the dominant cdc25.d1 allele, suppressed cut12.1. Thus, rot mutants provide a further link between protein production and cell-cycle progression.en
dc.language.isoenen
dc.subject.meshCell Cycle-
dc.subject.meshCloning, Molecular-
dc.subject.meshGene Expression Regulation, Fungal-
dc.subject.meshGenes, Fungal-
dc.subject.meshMicrotubule-Associated Proteins-
dc.subject.meshMitotic Spindle Apparatus-
dc.subject.meshMutant Proteins-
dc.subject.meshPhenotype-
dc.subject.meshPhosphoproteins-
dc.subject.meshProtein Biosynthesis-
dc.subject.meshSchizosaccharomyces-
dc.subject.meshSchizosaccharomyces pombe Proteins-
dc.subject.meshSuppression, Genetic-
dc.subject.meshTranscription, Genetic-
dc.subject.meshcdc25 Phosphatases-
dc.titleSuppression of the Schizosaccharomyces pombe cut12.1 cell-cycle defect by mutations in cdc25 and genes involved in transcriptional and translational control.en
dc.typeArticleen
dc.contributor.departmentCRUK Cell Division Group, Paterson Institute for Cancer Research, University of Manchester, Manchester M20 4BX, United Kingdom.en
dc.identifier.journalGeneticsen

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